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A Black Cohosh Extract Causes Hematologic and Biochemical Changes Consistent with a Functional Cobalamin Deficiency
Michelle C Cora1, William Gwinn1, Ralph Wilson1
11 Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, North Carolina, USA.
Black cohosh extract (BCE) may cause anemia by interfering with vitamin B12 absorption. This study found BCE increased markers of cobalamin deficiency in mice, suggesting a potential mechanism for its hematological effects.
Area of Science:
- Toxicology
- Hematology
- Nutritional Biochemistry
Background:
- Black cohosh rhizome is a popular dietary supplement for menopausal symptoms and dysmenorrhea.
- Previous studies indicated black cohosh dried ethanolic extract (BCE) can cause ineffective erythropoiesis and macrocytosis in female mice.
- This condition resembles megaloblastic anemia, prompting an investigation into its underlying mechanisms.
Purpose of the Study:
- To investigate the potential mechanisms by which BCE induces hematological changes.
- To determine if BCE affects folate and cobalamin metabolism.
- To explore the impact of BCE on homocysteine and methylmalonic acid levels.
Main Methods:
- Female B6C3F1/N mice were administered 1,000 mg/kg BCE or vehicle via gavage for 92 days.
- Comprehensive hematological and clinical chemistry analyses were performed on blood samples.
- Serum and red blood cell folate, serum cobalamin, plasma homocysteine, and methylmalonic acid (MMA) were measured.
- Folate levels in liver and kidney tissues were also assessed.
Main Results:
- BCE administration led to decreased red blood cell count and increased mean corpuscular volume.
- Significant reductions in reticulocyte, white blood cell, neutrophil, and lymphocyte counts were observed.
- Increased plasma homocysteine and MMA concentrations were detected in BCE-treated mice.
- Blood smear analysis revealed Howell-Jolly bodies and basophilic stippling in treated animals.
Conclusions:
- BCE exposure in mice induced hematological and clinical chemistry alterations consistent with functional cobalamin deficiency.
- The findings suggest a potential impact on folate metabolism as well.
- Further research is necessary to fully elucidate the mechanism behind BCE-induced increases in homocysteine and MMA.
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